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manganese/infarction
Veza se sprema u međuspremnik
Stranica 1 iz 177 rezultatima
Association of manganese superoxide dismutase Ala16Val polymorphism in the incidence of acute myocardial infarction in the Egyptians.
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Background: Oxidative stress has been implicated in various diseases including atherosclerosis; the most common pathologic process underlying acute myocardial infarction (AMI). The manganese superoxide dismutase (MnSOD) antioxidant enzyme affords the major defense against reactive oxygen
Characterization of viable and nonviable myocardium at MR imaging: comparison of gadolinium-based extracellular and blood pool contrast materials versus manganese-based contrast materials in a rat myocardial infarction model.
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OBJECTIVE
To determine the contrast agent behavior of gadolinium-based (extracellular and albumin-binding) and manganese-based contrast media for late-enhancement imaging of myocardial infarction.
METHODS
Coronary ligation was performed in 30 rats, and they were serially imaged with segmented
Association of manganese superoxide dismutase and glutathione S-transferases genotypes with myocardial infarction in patients with type 2 diabetes mellitus.
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OBJECTIVE
In the present study we investigated the association between genetic polymorphisms with functional effects on redox regulation: Val16Ala of manganese superoxide dismutase (MnSOD), polymorphic deletions of glutathione S-transferases M1 (GSTM1) and T1 (GSTT1) and Ile105Val of glutathione
Manganese dipyridoxyl-diphosphate (MnDPDP) as a viability marker in patients with myocardial infarction.
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OBJECTIVE
To evaluate contrast accumulation in left ventricular (LV) myocardium after manganese dipyridoxyl-diphosphate (MnDPDP) administration in patients with recent first time myocardial infarction.
METHODS
MnDPDP (5 micromol/kg) was administered to 10 patients with recent myocardial infarction
Accurate identification of myocardial viability after myocardial infarction with novel manganese chelate-based MR imaging.
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We developed a novel manganese (Mn2+ ) chelate for magnetic resonance imaging (MRI) assessment of myocardial viability in acute and chronic myocardial infarct (MI) models, and compared it with Gadolinium-based delay enhancement MRI (Gd3+ -DEMRI) and histology. MI was induced in
Chromium and manganese levels in biological samples of Pakistani myocardial infarction patients at different stages as related to controls.
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It has been speculated that trace elements may play a role in the pathogenesis of heart diseases In the present study, we aimed to access the levels of chromium (Cr) and manganese (Mn) in biological samples (whole blood, urine, and scalp hair) of myocardial infarction (MI) patients of both gender
Plasma and erythrocyte manganese concentrations. Influence of age and acute myocardial infarction.
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This study was carried out to assess manganese (Mn) status after an acute episode of myocardial infarction. Plasma and erythrocyte Mn concentrations were measured from admission to hospital to day 15 postadmission in 21 patients suffering from acute myocardial infarction and in three control groups.
In vivo myocardial infarct area at risk assessment in the rat using manganese enhanced magnetic resonance imaging (MEMRI) at 1.5T.
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The aim of this study was to measure the myocardial area at risk in rat, using MRI and manganese injection during a coronary occlusion/reperfusion model at 1.5T. A sequential protocol with occlusion and MnCl2 injection immediately followed by MRI was used with the assumption that MnCl2-induced
Myocardial viability of the peri-infarct region measured by T1 mapping post manganese-enhanced MRI correlates with LV dysfunction.
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Influence of myocardial infarction on serum manganese, copper, and zinc concentrations.
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Reportedly, serum manganese concentrations increase after myocardial infarction, closely correlated with increased serum aspartate aminotransferase activity. However, these conclusions are apparently based on analyses of contaminated samples. Serum manganese concentrations after myocardial
Indirectly probing Ca(2+) handling alterations following myocardial infarction in a murine model using T(1)-mapping manganese-enhanced magnetic resonance imaging.
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Prolonged ischemia causes cellular necrosis and myocardial infarction (MI) via intracellular calcium (Ca(2+)) overload. Manganese-enhanced MRI indirectly assesses Ca(2+) influx movement in vivo as manganese (Mn(2+)) is a Ca(2+) analog. To characterize myocardial Mn(2+) efflux properties,
Myocardial infarction quantification with Manganese-Enhanced MRI (MEMRI) in mice using a 3T clinical scanner.
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Manganese (Mn(2+)) was recognized early as an efficient intracellular MR contrast agent to assess cardiomyocyte viability. It had previously been used for the assessment of myocardial infarction in various animal models from pig to mouse. However, whether Manganese-Enhanced MRI (MEMRI) is also able
Monitoring dynamic alterations in calcium homeostasis by T (1)-weighted and T (1)-mapping cardiac manganese-enhanced MRI in a murine myocardial infarction model.
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Manganese has been used as a T(1)-weighted MRI contrast agent in a variety of applications. Because manganese ions (Mn(2+)) enter viable myocardial cells via voltage-gated Ca(2+) channels, manganese-enhanced MRI is sensitive to the viability and inotropic state of the heart. In spite of the
Simultaneous assessment of left-ventricular infarction size, function and tissue viability in a murine model of myocardial infarction by cardiac manganese-enhanced magnetic resonance imaging (MEMRI).
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Owing to its signal-enhancing characteristics in viable well-perfused tissue, divalent manganese (Mn2+) has been used as a myocardial imaging contrast agent. Because Mn2+ can enter excitable cells through the voltage-gated L-type calcium channels, manganese-enhanced MRI (MEMRI) has been used to
Magnetic resonance imaging of myocardial infarction using a manganese-based contrast agent (EVP 1001-1): preliminary results in a dog model.
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OBJECTIVE
To investigate the MRI characteristics of an intracellular manganese-based contrast agent, EVP 1001-1 (Eagle Vision Pharmaceutical Corp.), in a canine model of myocardial infarction.
METHODS
Three dogs were imaged 14-37 days following permanent ligation of the left anterior descending
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